| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| ln Vitro |
With an IC50 of 40 μM, acetylshikonin (1.6-100 μM) suppresses the growth of the KB-R5 oral cancer cell [6]. In KB-R5 cells, acetylshikonin (20–80 μM; 24 h) can cause apoptosis and (20–80 μM) autophagy in addition to blocking the mTOR/PI3K/AKT signaling pathway [6]. By upregulating heme oxygenase-1, acetylshikonin (1-10 μM; 12 h) can prevent H2O2 (500 μM; 4 h)-induced apoptosis in neuroblastoma SH-SY5Y and pc12 cells [8]. The anti-Coxsackievirus A16 (CVA16) action of acetylshikonin (0.01-5 μM/L; 2 h) is observed during the adsorption/invasion phase with an EC50 of 0.04 μmol/L. However, it is not effective during the pre-infection, replication, or release phases of the virus [2]. Through PLC-β3/PKCδ mediation, acetylshikonin (0.01-1 μM; 30 min) increases glucose absorption by skeletal muscle cells L6 to lower blood glucose levels [3]. In HK2 cells, acetylshikonin (1–5 μg/mL); 48 h) can prevent renal fibrosis brought on by TGF-β1 (5 ng/mL) [5].
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| ln Vivo |
In BALB/c nude mice, acetylshikonin (50 mg/kg; intraperitoneal injection; three times a week for six weeks) significantly and concentration-dependently reduced the formation of tumors [6]. Acetylshikonin (270–1080 mg/kg; gavage; once daily for 30 days) decreases hippocampus aging and cognitive impairment caused by d-galactose (150 mg/kg) [1]. In mice, acetylshikonin (2 mg/kg; IM; single dosage) suppresses the replication of coxsackievirus 16 (CVA16) [2]. Acetylshikonin (100 mg/kg; gavage; once daily for eight weeks) can effectively suppress renal fibrosis and reduce impairment to renal function by inhibiting the TGF-β1/Smad pathway [5]. When alloxan (180 mg/kg; i.p.; single dosage) is administered to mice with diabetes, acetylshikonin (10 mk/kg; i.p.; once daily for three consecutive days) lowers blood glucose levels [3]. In obese C57BL/6J mice, acetylshikonin (540 mg/kg; PO; once daily for eight weeks) decreases the formation of hepatic fat via controlling fat metabolism and liver inflammation, improving obesity and non-alcoholic fatty liver disease (NAFLD) [4]. Acetylshikonin (120–1080 mg/kg; gavage;) can inhibit rat pregnancy ability by affecting gonadotropin (GTH) secretion and lowering serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). It has no effect on Sprague-Dawley rats at low doses (120 mg/kg and 360 mg/kg) and no effect on pregnancy at high doses (1080 mg/kg) [7].
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| Cell Assay |
Apoptosis Analysis[6]
Cell Types: KB-R5 (oral cancer cell line) Tested Concentrations: 20 μM, 40 μM, 80 μM Incubation Duration: 24 h Experimental Results: Changed the morphology of the nucleus. Increased apoptosis ratio. Western Blot Analysis[6] Cell Types: KB-R5 (oral cancer cell line) Tested Concentrations: 20 μM, 40 μM, 80 μM Incubation Duration: Experimental Results: Increased the expression of Beclin-1 and LC3-II and inhibited the expression of p62. However, had no effect on the expression of LC3-I and Vps34. diminished the expression of p-mTOR, p-PI3K and p-AKT in a concentration-dependent manner. Cell Viability Assay[2] Cell Types: CVA16-induced human rhabdomyosarcoma (RD) cells Tested Concentrations: 0.01-5 μM/L (1:1 mix with CVA16 strain TA271) Incubation Duration: 2 h Experimental Results: decreased CVA16-induced cytopathic effect with inhibition rates of 80% at the concentration of 0.08 μmol/L. Western Blot Analysis [3] Cell Types: L6 (rat skeletal muscle cells) Tested Concentrations: 0.01 μM, 0.1 μM, 1 μM Incubation Duration: 2 h Experimental Results: Dramatically up-regulated phos |
| Animal Protocol |
Animal/Disease Models: D-galactose (D-gal)-induced sub-acuteaging mouse model of Alzheimer's disease (AD)[1]
Doses: 270 mg/kg, 540 mg/kg, 1080 mg/kg Route of Administration: intragastric (po) administration (ig) ; one time/day for 30 days. After D-gal treatment (150 mg/kg; subcutaneous (sc) injection; one time/day for 30 days) Experimental Results: diminished levels of the pro-inflammatory cytokines IL-1β and TNF-α. diminished the content of MDA and increased the activity of SOD. Dramatically mitigated D-Gal-induced downregulation of SIRT1 in hippocampal neurons. Dramatically inhibited the expression of p53, acetyl-p53, and p21 in mice (all proteins associated with hippocampal aging). Animal/Disease Models: CAV16-indeced ICR suckling mice model[2] Doses: 2 mg/kg Route of Administration: intramuscular (im) injection; Single dose. After CVA16 treatment (10[5.5] TCID50/g; intramuscular (im) injection; Single dose ) Experimental Results: Delayed death of the mice (6 days post-infection and 7 dpi), and eventually resulted in a survival rate of 50% and 70% for |
| References |
[1]. Park SH, et al. Identification of acetylshikonin as the novel CYP2J2 inhibitor with anti-cancer activity in HepG2 cells. Phytomedicine. 2017 Jan 15;24:134-140.
[2]. Shon JC, et al. Acetylshikonin is a novel non-selective cytochrome P450 inhibitor. Biopharm Drug Dispos. 2017 Dec;38(9):553-556. [3]. Wang Y, et al. Acetylshikonin, a Novel AChE Inhibitor, Inhibits Apoptosis via Upregulation of Heme Oxygenase-1 Expression in SH-SY5Y Cells. Evid Based Complement Alternat Med. 2013;2013:937370. |
| Molecular Formula |
C18H18O6
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| Molecular Weight |
337.3751
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| CAS # |
24502-78-1
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| Related CAS # |
DL-Acetylshikonin;54984-93-9
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| SMILES |
O(C(C([H])([H])[H])=O)C([H])(C([H])([H])/C(/[2H])=C(\C([2H])([2H])[2H])/C([2H])([2H])[2H])C1=C([H])C(C2=C(C([H])=C([H])C(=C2C1=O)O[H])O[H])=O
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~50 mg/mL (~151.36 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.57 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9640 mL | 14.8201 mL | 29.6402 mL | |
| 5 mM | 0.5928 mL | 2.9640 mL | 5.9280 mL | |
| 10 mM | 0.2964 mL | 1.4820 mL | 2.9640 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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